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Cardiovascular System

The cardiovascular system is also called the circulatory system or the blood-vascular system. It is primarily responsible for transporting oxygen among many other important substances and nutrients throughout the body. The heart, a powerful pump, utilizes an intricate and extensive network of blood vessels to perform this function.

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Anatomy of the Heart

Anatomical Location of the Heart

  • Snugly enclosed within the middle mediastinum (medial cavity of thorax), which contains the
    • Heart
    • Pericardium
    • Great Vessels
    • Trachea
    • Esophagus
  • Middle Mediastinum – located in the inferior mediastinum (lower than the sternal angle)
  • Extends obliquely from 2nd rib → 5th intercostal space
  • Anterior to Vertebrae
  • Posterior to Sternum
  • Flanked by 2 lungs
  • Rests on the diaphragm
  • 2/3 of its mass lies to the LHS of the midsternal line

The Pericardium (Coverings of the Heart)

  • A double-walled sac
  • Contains a film of lubricating serous fluid
  • 2 Layers of Pericardium
    • Fibrous Pericardium
      • Tough, dense connective tissue
      • Protects the heart
      • Anchors it to surrounding structures
      • Prevents overfilling of the heart – if fluid builds up in the pericardial cavity, it can inhibit effective pumping. (Cardiac Tamponade)
    • Serous Pericardium (one continuous sheet with ‘2 layers’)
      • Parietal Layer – Lines the internal surface of the fibrous pericardium
      • Visceral Layer – (aka Epicardium) Lines the external heart surface

Layers of the Heart Wall 

  • Epicardium
    • Visceral layer of serous pericardium
  • Myocardium
    • Muscle of the heart
    • The layer that ‘contracts’
  • Endocardium
    • Lines the chambers of the heart (endothelial cells)
    • Prevents clotting of blood within the heart
    • Forms a barrier between the O2 hungry myocardium and the blood (blood is supplied via the coronary system)

Fibrous Skeleton of the Heart

  • The network of connective tissue fibers (collagen & elastin) within the myocardium
  • Anchors the cardiac muscle fibers + valves + great vessels.
  • Reinforces the myocardium
  • Provides electrical isolation
  • 2 parts
    • Septum
      • Flat sheets separating atriums, ventricles & left and right sides of the heart
      • Electrically isolates the left & right sides of the heart (connective tissue = non-conductive)
        • Important for cardiac cycle
      • Interatrial septum/atrioventricular septum/interventricular septum
    • Ring
      • Rings around great vessel entrances & valves
      • Stops stretching under pressure 

Chambers & Associated Great Vessels

2 Atria (Superior) 

  • Atrium = entryway
  • On the superior aspect of the heart (above the ventricles)
  • Each has a small, protruding appendage called auricles – increasing atrial volume
  • Separated by Atrial Septum (Site of Fetal Shunt Foramen Ovale)
  • Right Atrium
    • Ridged internal anterior wall – due to muscle bundles called pectinate muscles
    • Blood enters via 3 veins
      • Superior Vena Cava
      • Inferior Vena Cava
      • Coronary Sinus (collects blood draining from the myocardium)
  • Left Atrium
  • Blood enters via
    • The 4 pulmonary veins (O2 blood)


2 Ventricles (Inferior) 

  • Vent = underside
  • Thick, muscular Discharging Chambers
  • The ‘pumps’ of the heart
  • Trabeculae Carneae (crossbars of flesh) line the internal walls
  • Papillary Muscles play a role in valve function
  • Right Ventricle
    • Most of heart’s Anterior Surface
    • Thinner – responsible for the Pulmonary Circulation – Via Pulmonary Trunk
  • Left Ventricle
    • Most of the heart’s Postero-Inferior Surface
    • Thicker – it is responsible for the Systemic Circulation – Via Aorta

Landmarks of the Heart

  • Coronary Sulcus (Atrioventricular Groove)
    • Encircles the junction between the Atria & Ventricles like a ‘Crown’ (Corona)
    • Cradles the Coronary Arteries (R&L), Coronary Sinus, & Great Cardiac Vein
  • Anterior Interventricular Sulcus
    • Cradles the Anterior Interventricular Artery (Left Anterior Descending Artery)
    • Separates the right & left Ventricles anteriorly
    • Continues as the posterior Interventricular Sulcus
  • Posterior Interventricular Sulcus
    • Cradles the Posterior Descending Artery
    • Continuation of the Anterior Interventricular Sulcus
    • Separates the right & left ventricles posteriorly

Pathway of Blood through the Heart

The right side

  • pumps blood through the pulmonary circuit (to the lungs and back to the left side of the heart)
  • blood flowing through the pulmonary circuit gains oxygen and loses carbon dioxide, indicated by the color change from blue to red

The left side

  • pumps blood via the systemic circuit to all body tissues and back to the right side of the heart
  • blood flowing through the systemic circuit loses oxygen and picks up carbon dioxide (red to blue color change)

Coronary Circulation

  • The myocardium’s own blood supply
  • The shortest circulation in the body
  • Arteries lie in epicardium – prevents the contractions inhibiting blood flow
  • There is a lot of variation among different people

Arterial Supply

  • Encircle the heart in the coronary sulcus
  • Aorta → Left & Right coronary arteries
    • Left Coronary Artery → 2 Branches:
  1. Anterior Interventricular Artery (aka. Left Anterior Descending Artery or LAD
  • Follows the Anterior InterVentricular Sulcus
  • Supplies Apex, Anterior LV, Anterior 2/3 of IV-Septum
  1. Circumflex Artery
  • Follows the Coronary Sulcus (aka. AtrioVentricular Groove)
  • Supplies the Left Atrium + Lateral LV
  • Right Coronary Artery → 2 (‘T-junction) Branches:
    • Marginal Artery:
      • Serves the Myocardium Lateral RHS of Heart
  • Posterior Interventricular Artery:
    • Supplies posterior ventricular walls
    • Anastomoses with the Anterior Interventricular Artery (LAD)

Venous Drainage 

  • Venous blood – collected by the Cardiac Veins (empties into the right atrium)
    • Great Cardiac Vein (in Anterior InterVentricular Sulcus)
    • Middle Cardiac Vein (in Posterior InterVentricular Sulcus)
    • Small Cardiac Vein (along Right inferior Margin)

Heart Valves

Ensure unidirectional flow of blood through the heart

2x Atrioventricular (AV) (Cuspid) Valves

  • Location → at the 2 atrial-ventricular junctions
  • Function → prevent backflow into the atria during contraction of ventricles
  • Chordae tendineae (tendinous cords) “heart strings” – attached to each valve flap
    • Anchor the cusps to the Papillary Muscles protruding from ventricular walls.
      • Papillary muscles contract before the ventricle to tension the chordae tendineae
      • Prevent inversion of valves under ventricular contraction
  • Tricuspid valve (right)
    • 3 flexible ‘cusps’ (flaps of endocardium + Conn. Tissue)
  • Mitral valve (left)
    • (resembles the 2-sided bishop’s mitre [hat])

2x Semilunar (SL) Valves

  • Located at the bases of both large arteries issuing from the ventricles
  • Each consists of 3 pocket-like cusps resembling a crescent moon (semilunar = half moon)
  • Open under Ventricular Pressure
  • Pulmonary Valve
    • Between Right Ventricle & Pulmonary Trunk
  • Aortic Valve
    • Between Left Ventricle & Aorta

Valve Positions during ventricular contraction (left) and relaxation (right)


Valve Sounds

  1. “Lubb”
  • Sound of AV valve closure
  • M1 = Mitral component
  • T1 = Tricuspid component
  1. “Dupp”
  • Sound of SL valve closure
  • A2 = Aortic component
  • P2 = Pulmonary component

Electrophysiology of the Heart

The Heartbeat

  • Heart is a muscle and requires
    • O2,
    • Nutrients, and
    • Action Potentials to function
      • However, these neural signals don’t come from the brain;
      • Rather, the heart has its own conduction systems
        • allow heart to contract autonomously
      • Hence why a transplanted heart still operates (if provided with O2 and nutrients)
  • Cardiac Activity is coordinated:
    • To be effective, the atria & ventricles must contract in a coordinated manner
    • This activity is coordinated by the heart’s Conduction Systems
  • The entire heart is electrically connected by:
    • Gap junctions
      • Allow action potentials to move from cell to cell
    • Intercalated discs
      • Support synchronized contraction of cardiac tissue

The Heart’s Conduction Systems

SA Node → AV Node → Bundle of His → R&L Bundle Branches → Purkinje Fibers → Myocyte Contraction

Conductile Cardiac Cell Physiology (SA/AV Node Cells)

  • Action Potentials: Slow ‘Pacemaker’ Type
  • Have UNSTABLE Resting Membrane Potentials → spontaneous electrical activity
    • Spontaneously depolarize to threshold
      • This gradual depolarisation is called a ‘Prepotential’
      • Due to leaky Na+ membrane ion channels
      • Therefore – firing frequency depends on Na+ movement
    • Depolarisation:
      • Once threshold is reached, Ca2+ channels open
      • → Influx of Ca+
      • → Causes an action potential
    • Repolarisation:
      • Once peak MP is reached, Ca+ channels close, K+ channels open
      • → K+ Efflux makes MP more negative
  • → Causes repolarisation
  • (Na+ brings to threshold, but Ca+ is responsible for Depolarisation.)
  • With a Hierarchy of control over the heart
    • Hierarchy based on natural intrinsic rate (fastest node (SA node) takes control)

Contractile Cardiac Cell Physiology (Purkinje Fibers & Myocytes)

  • Action Potentials: Fast ‘Non-Pacemaker’ Type
  • Have STABLE Resting Membrane Potentials
    • Resting Membrane Potential (MP):
      • Na+ & Ca+ channels are closed
      • Any positive change to MP causes Fast Na+ channels to open → positive feedback → threshold
    • Depolarisation:
      • If MP reaches threshold, all Fast Na+ channels open;
      • → Massive influx of Na+ into cell
      • → Membrane depolarises
    • Plateau:
      • Fast Na+ channels inactivate
      • → The small downward deflection is due to Efflux of K+ ions
      • → Action potential causes membrane Voltage-Gated Ca+ channels to open
        • This triggers further Ca+ release by the sarcoplasmic reticulum into the sarcoplasm (“Ca induced Ca Release”)
          • This increased myoplasmic Ca+ causes muscular contraction.
        • Plateau is sustained by influx of Ca+, balanced by efflux of K+ ions
    • Repolarization:
      • Influxing Ca+ channels close, the effluxing K+ channels remain open
        • → Result is a net outward flow of positive charge. → Downward Deflection
        • → As the MP falls, more K+ channels open, accelerating depolarization
        • → Membrane Repolarizes & most of the K+ channels close
    • What happens to the excess ions?
      • Excess Na+ in the cell from depolarization is removed by the Na/K-ATPase
      • Deficit of K+ in the cell from repolarization is replaced by the Na/K-ATPase
      • Excess Ca+ from the Plateau Phase is eliminated by a Na/Ca Exchanger


There is considerable delay between myocardial contraction and the action potential.

Refractory Periods

In cardiac muscle, the Absolute Refractory Period continues until muscle relaxation

  • Therefore, summation is not possible → tetany cannot occur (critical in heart)
  • i.e., the depolarized cell will not respond to a 2nd stimulus until contraction is finished

Absolute Refractory Period 

  • Approximately 200ms
  • Duration: from peak → plateau → halfway-polarized 

Relative Refractory Period 

  • Na+ channels are closed – but can still respond to a stronger-than-normal stimulus
  • Approximately 50ms
  • Duration: last half of repolarization 

The Sinoatrial (SA) Node

  • The “Pacemaker” of the Heart: Unregulated Rate: 90-100bpm; however
    • Parasympathetic NS lowers heart rate → keeps Normal Resting HR at 70bpm
    • Sympathetic NS raises heart rate
  • Location
    • Posterior Wall of the Right Atrium near the opening of the Superior Vena Cava
  • Nature of Action Potentials
    • Continually Depolarizing 90-100bpm
    • Takes 50ms for Action-Potential to reach the AV Node
  • Role in Conduction Network
    • Sets the pace for the heart as a whole
  • Portion of Myocardium Served
    • Contracts the Right & Left Atrium

The Atrioventricular (AV) Node

  • 2nd in Command: Slower than the SA Node: 40-60bpm
  • Location
    • Inferior portion of the Interatrial Septum
    • Directly above the Tricuspid Valve
  • Nature of Action Potentials
    • Continually Depolarizing – but slower than the SA Node (40-60 bpm)
  • Role in Conduction Network
    • To delay the impulse from the Sinoatrial Node → bundle branches;
    • Delay allows the atria to empty their contents before Ventricular Contraction
    • Delay: approx. 100ms
  • Portion of Myocardium served
    • Conducts the SA Node impulses to the Purkinje Fibers (which supply the ventricular walls)

Bundle Branches (Bundles of His)

  • 3rd in Command: slower than AV & SA Nodes: 20–40 bpm
  • Location
    • Fork of branches – superior portion of interventricular septum 
  • Nature of Action Potentials
    • Continually depolarizing – slower than AV & SA Nodes (20–40 bpm)
  • Role in conduction network 
    • Serves as the only connection between the 2 atria & 2 ventricles
    • The 2 atria & 2 ventricles are isolated by the fibrous skeleton and lack of gap junctions
  • Portion of the myocardium served 
    • Transmits impulses from the AV node to the R&L Bundle branches 
    • Then along the interventricular septum → apex of the heart 

Purkinje Fibers 

  • Specialized Myocytes with very few myofibrils → don’t contract during impulse transmission
  • Location
    • The Inner Ventricular Walls of the Heart – just below the Endocardium
    • Begin at the heart apex, then turn superiorly into the Ventricular Walls
  • Nature of Action Potentials
    • Conductile
    • Resembles those of Ventricular Myocardial Fibers
      • However the Depolarisation is more pronounced & the Plateau is longer.
      • Long Refractory period
    • Capable of Spontaneous Depolarisation – 15bpm
  • Role in Conduction Network
    • Carry the contraction impulse from the L & R Bundle Branches to the Myocardium of the Ventricles
    • Causes Ventricles to contract
  • Portion of Myocardium served
    • R & L Ventricles
  SA Node AV Node Bundles of His Purkinje Fibers
Description “Pacemaker” of the Heart 2nd in command  3rd in command  Specialized myocytes with very few myofibrils (do not contract during impulse transmission)
Rate (bpm) 90-100 40-60 20-40 N/A
Location Posterior wall of the right atrium; near opening of Superior Vena Cava Inferior portion of the interatrial septum; directly above the tricuspid valve  Fork of branches; superior portion of interventricular septum Inner ventricular walls of the heart (just below the endocardium); begin at the heart apex, then turn superiorly into the ventricular walls
Nature of Action Potentials Continually depolarizing (90-100bpm); takes 50ms for action potential to reach AV node  Continually depolarizing (slower than the SA node)  Continually depolarizing (slower than AV & SA nodes)  Conductile (resembles ventricular myocardial fibers); more pronounced depolarization; longer plateau; longer refractory period 
Role in Conduction Network Sets the pace for the heart as a whole Delay the impulse from the SA node → Bundle branches (100ms) Serves as the only connection between the 2 atria and 2 ventricles (these are isolated by the fibrous skeleton and lack of gap junctions) Carry the contraction impulse from the left and right Bundle branches to the myocardium of the ventricles; causes ventricles to contract
Portion of Myocardium Served Contracts the right and left atria Conducts the SA node impulses to the Purkinje Fibers  Transmits impulses from the AV node to the right and left Bundle branches; then along the interventricular septum → apex of the heart Right and left ventricles 

Effect of the Autonomic Nervous System (ANS)

Although the heart can operate on its own, it normally communicates with the brain via the autonomic nervous system

Parasympathetic Nervous System 

  • Innervates SA & AV Nodes → slows heart rate
  • Direct Stimulation → Releases Acetylcholine → Muscarinic receptors in SA/AV Nodes
    • Causes increased K+ permeability (Efflux) → Hyperpolarizes the cell
      • Cell takes longer to reach threshold → Lower Heart Rate

Sympathetic Nervous System

  • Innervates the SA & AV Nodes & ventricular muscle
    • → Raises Heart Rate
    • → Increases force of contraction
    • → Dilates arteries
  • Indirect stimulation → Sympathetic nerve fibers release Noradrenaline (Norepinephrine) at their cardiac synapses → Binds to Beta 1 Receptors on Nodes & Muscles →
    • Initiates a cyclic AMP pathway → Increases Na+ + Ca+ permeability in nodal tissue & increases Ca+ permeability(Membrane & SR) in muscle tissue
  • Effects on Nodal Tissue
    • ++Permeability to Na+ → more influx of Na+ → Membrane ‘drifts’ quicker to threshold → Increased heart rate
    • ++Permeability to Ca+ → more influx of Ca+ → Membrane depolarisation is quicker → Increased heart rate
  • Effects on Contractile Tissue
    • ++ Membrane permeability to Ca+ → More influx of Ca+
    • ++Sarcoplasmic reticulum permeability to Ca+ → Efflux of Ca+ into cytoplasm→
      • Increases available Ca+ for contraction → Contractile force increases

Electrocardiogram (ECG) Physiology 

What is an ECG?

  • A recording of all action potentials by nodal & contractile cells in the heart at a given time 
    • It i NOT a single action potential 
    • A “lead” refers to a combination of electrodes that form an imaginary line in the body, along which the electrical signals are measured
      • i.e., a 12 ‘lead’ ECG usually only uses 10 electrodes 
  • Measured by voltmeters → record electrical potential across 2 points
    • 3x bipolar leads: measure voltages between the arms or between an arm and a leg
      • I = LA(+) RA(-)
      • II = LL(+) RA(-)
      • III = LL(+) LA(-)
    • 9x unipolar leads: look at the heart in a ‘3D’ image 
  • Graphic output
    • X-axis: time 
    • Y-axis: amplitude (voltage) – proportional to number and size of cells 
  • Understanding waveforms 
    • When a Depolarisation Wavefront moves toward a positive electrode, a Positive deflection results in the corresponding lead.
    • When a Depolarisation Wavefront moves away from a positive electrode, a Negative deflection results in the corresponding lead.
    • When a Depolarisation Wavefront moves perpendicular to a positive electrode, it first creates a positive deflection, then a negative deflection.

How Each Wave Segment is Formed

Depolarization of the atria 
Presence of this wave indicates the SA node is working
Reflects the delay between SA & AV nodes
Atrial contraction is occurring at this time 
Interventricular septum depolarization 
Wave direction (see blue arrow) is perpendicular to the main electrical axis → results in a biphasic trace
Only the negative deflection is seen due to signal cancellation by atrial repolarization 
Sometimes this wave isn’t seen at all
Ventricular depolarization 
Wave direction (see blue arrow) is the same as the main electrical axis → positive deflection 
R-wave amplitude is large due to sheer numbers of depolarizing myocytes
Depolarization of the myocytes at the last of the
Purkinje Fibers 
Wave direction (black arrow) opposes the main electrical axis → negative deflection 
This wave is not always seen 
Ventricular contraction is occurring at this time
Due to the lag between excitation and contraction
Ventricular repolarization 
Positive deflection despite being a repolarization wave – because repolarization waves travel in the opposite direction to depolarization waves

Relating ECG Waves to Events in the Cardiac Cycle 

  • Contractions of the heart ALWAYS lag behind impulses seen on the ECG
  • Fluids move from high → low pressure 
  • Heart valves ensure a unidirectional flow of blood 
  • Coordinated contraction timing – critical for correct flow of blood 

The Heart’s Electrical Axis 

  • Refers to the general direction of the heart’s depolarization wavefront (or ‘mean electrical vector’) in the frontal plane
    • It is usually oriented in a ‘Right Shoulder to Left Leg’ direction
  • Determining the electrical axis from an ECG trace
    • 3 methods
      • Quadrant Method (the one you’re concerned with)
      • Peak Height Measurement Method
      • The Degree Method

The Quadrant Method 

+ + Normal(0 to +90°)
+ **Possible LAD (0 to -90°)
+ RAD (+90° to 180°)
Extreme Axis(-90° to 180°)
  • Normal Axis. QRS positive in I and aVF (0 90 degrees). Normal axis is actually 30 to 105 degrees.
  • Left Axis Deviation (LAD). QRS positive in I and negative in aVF, 30 to 90 degrees
  • Right Axis Deviation (RAD). QRS negative in I and positive in aVF, +105 to +180 degrees
  • Extreme RAD. QRS negative in I and negative in aVF, +180 to +270 or 90 to 180 degrees

Algorithm for Looking at ECGs

  • Check Pt ID
  • Check voltage & timing
    • 25mm/sec
    • 1 large square = 0.2s (1/5sec)
    • 1 small square = 0.04s
  • What is the rate?
    • 300/number of large squares between QRS Complexes
      • Tachycardia >100bpm
      • Bradycardia <60bpm
  • What is the rhythm?
    • Sinus? (are there P-Waves before each QRS complex)
    • If not sinus?
      • Is it regular?
      • Irregular?
      • Irregularly Irregular (AF)
      • Brady/Tachy
  • Atrial Fibrillation
    • Irregularly Irregular
    • P-Waves at 300/min
  • QRS
    • Is there one QRS for each P-wave?
    • Long PR Interval? (1st degree heart block)
    • Missed Beats? (Second degree block)
    • No relationship? Complete heart block
  • Look for QRS Complexes
    • How wide – should be < 3 squares
    • If wide – It is most likely Ventricular
    • (Sometimes atrial with aberrant conduction (LBBB/RBBB)
    • IF Tachycardia, & Wide Complex → VT is most likely. (If hypotensive → Shock; if Normotensive → IV Drugs)
  • Look for T-Waves
    • Upright or Inverted
  • Look at ST-Segment
    • Raised, depressed, or inverted
    • ST Distribution → Tells you which of the coronaries are blocked/damaged
      • Inferior ischaemia (II, III, AVF)
      • Lateral ischaemia (I, II, AVL, V5, V6)
      • Anterior ischaemia (V, leads 2-6)
    • NOTE: Normal ECG Doesn’t exclude infarct.
    • ST Depression → Ischaemia
    • ST Elevation → Infarction
    • If LBBB or Paced, you CANNOT comment on ST-Segment

Mechanical Events of the Cardiac Cycle

Structure-Function Relationship of the Heart

  • The Myocardium is essentially one long muscle orientated in a spiral-like fashion
    • This allows the heart to be electrically integrated
    • Allows the heart to ‘wring out’ the blood within it
    • This setup facilitates a strong pumping action 


  • Systole = Myocardial Contraction
  • Diastole = Myocardial Relaxation
  • Stroke Volume = Output of Blood from the heart per contraction (≈80mL of blood)
  • Heart Rate = #Heart Beats/Minute
  • Cardiac Output
    • Volume of blood ejected from the heart per minute (Typically ≈5L/min)
    • Cardiac Output = Heart Rate x Stroke Volume
    • Chronotropic Influences
      • Affect heart rate
    • Inotropic Influences
      • Affect contractility (& stroke volume)
    • Dromotropic Influences
      • Affect AV Node delay
  • End Diastolic Volume = Ventricular volume at end of Diastole (When ventricle is fullest)
  • End Systolic Volume = Ventricular volume after Contraction (Normal ≈ 60-65%)
  • Preload = The degree of stretching of the heart muscle during Ventricular Diastole
    • (↑Preload = ↑cross linking of myofibrils = ↑Contraction (“Frank Starling Mechanism”)
  • Afterload = The ventricular pressure required to eject blood into aorta/pulmonary artery
    • (↑Afterload = ↓SV due to ↓ejection time)

Overview of the Cardiac Cycle

Phase 1 – Atrial Contraction (Systole) + Ventricular Filling (Diastole) 

  • Contraction of atria 
    • → intra-atrial pressure increases
    • → blood pushed into ventricles through AV valves 
  • Note: ventricles are already 70% full from passive venous filling 
  • At the end of atrial systole, ventricles have EDV (end diastolic volume) ≈130mL

Phase 2 – Ventricular Systole

AV Valves Close

  • Ventricular pressure exceeds atrial pressure → AV valves shut 
  • Brief period of isovolumetric contraction
    • Where ventricular pressure rises, but volume stays constant 
    • The beginning of ventricular systole
    • All valves are still closed 

Semilunar Valves Open 

  • Ventricular pressure exceeds aortic/pulmonary pressure → blood ejected
    • ≈80mL of blood ejected each time (Stroke Volume) 
    • Ventricular volume decreases

Semilunar Valves Close

  • Ventricular pressure then falls below aortic/pulmonary pressure → semilunar valves close
    • Sudden closure of semilunar valves causes the dicrotic notch
      • Result of elasticity of the aorta & blood rebounding off the closed SL valve 
      • Causes a slight peak in aortic pressure 
  • Note: ventricles never fully empty
    • ESV (End Systolic Volume) = amount of blood left in ventricles → 50mL

Phase 3 – Ventricular Diastole 

  • Ventricles relax → Ventricular pressure falls below atrial pressure → AV valves open:
    • Blood → from Atria into ventricles
    • (NOTE: Passive filling from venous return is responsible for 70% of ventricular filling.)


Cardiac Output

  • Useful when examining cardiac function over time
  • Determined by 2 things
    • Stroke Volume
    • Heart Rate

Cardiac Output(mL/min) = Stroke Volume X Heart Rate

  • Average CO ≈ 5L/min (i.e.: The entire blood supply circulates once per minute)
  • Cardiac Output is regulated such that peripheral tissues receive adequate blood supply

Heart Rate

  • Depends on tissue-satisfaction with nutrients and O2
  • Terms
    • Bradycardia. HR slower than normal (too fast → stroke volume & CO suffer) 
    • Tachycardia. HR faster than normal 

5 Things that Affect Heart Rate

  • Alterations in SA Node Firing 
    • SA node is the pacemaker; therefore, change it rate → change heart rate
      • → change CO 
  • Autonomic Nervous System
    • Parasympathetic (Vagus Nerve)
      • Decrease HR (negative chronotropic effect) 
      • Increase AV node delay (negative dromotropic effect) 
    • Sympathetic (Sympathetic Chains)
      • Increase HR (positive chronotropic effect) 
      • Increase force of contraction (positive inotropic effect) 
  • Reflex Controls 
    • Bainbridge Reflex (Atrial Walls)
      • Where an ↑Venous Return → ↑Heart Rate
      • (Stretch of Atrial Walls → Stretch Receptors → Sympathetic NS → ↑HR)
      • Responsible for 40-60% of HR increases
    • Chemoreceptor Reflex
      • ↓Low O2 or ↑CO2 in Peripheral-Tissue → ↑HR & ↑Respiratory Rate
    • Baroreceptor Reflex (Aortic & Carotids)
      • Where an ↑BP → ↓HR & ↓Contractility (+ Vasodilation)
      • 2 Main Baroreceptors
        • Aortic → Vagus Nerve → CV Center (medulla/pons)
        • Carotid → Hering’s Nerve → CV Center (medulla/pons)
      • Constantly responds to blood pressure change
        • (via stretch in vessel walls)
        • More stretch = More firing: leads to:
          • Parasympathetic activation
          • Sympathetic deactivation
      • Receptors never silent – constantly signaling
      • Quick to respond
      • In hypertension → receptors recalibrate to the higher BP
      • Changes HR accordingly
  • Atrial Node Stretching (similar to baroreceptor reflex, but in the atrium)
    • Venous return fills atria with blood
      • When Venous Return ↑, Atrial Walls Stretch → Stretches SA-Node
    • Stretching of SA node cells → More rapid depolarisation → ↑HR
    • Responsible for 15% of HR increases
    • Influenced by
      • Arterial Pressure
      • Peripheral Compliance
      • Local Blood Flow
      • Capillary Exchange
  • Chemical Regulation 
    • Hormones
      • Adrenaline 
      • Thyroxine 
      • Insulin 
    • Ions
      • Na+
      • K+
      • Ca2+

Other Factors that Affect HR 

  • Age (old → lower resting HR) 
  • Gender (females → higher resting HR) 
  • Physical fitness (fit → lower resting HR) 
  • Temperature (hot → higher resting HR) 

Stroke Volume

  • Blood output per heartbeat
  • Useful when examining the efficiency of a single cardiac cycle

Stroke Volume (SV) = End Diastolic Volume (EDV) – End Systolic Volume (ESV)

  • Therefore, Stroke Volume is ↑ by
    • ↑ Ventricular filling time (duration of ventricular diastole)
    • ↑ Venous return
    • ↓ Arterial BP (a high arterial BP → harder to eject blood → ESV increases)
    • ↑ Force of ventricular contraction

2 Things that Affect Stroke Volume 


  • The degree of stretching of the heart muscle during Ventricular Diastole
  • Caused by amounts of blood from venous return
  • Influenced by
    • Arterial Pressure
    • Peripheral Compliance
    • Local Blood Flow (depending on the demands of those tissues)
    • Capillary Exchange.
  • Preload ↑ as EDV↑ (directly proportional)
    • ↑End Diastolic Volume = ↑Stroke Volume (Frank-Starling Law)
  • Affects % of actin/myosin contact in myocytes→ Affects cross-bridge cycling:
    • → Affects muscle’s ability to produce tension
    • Preload varies with demands placed on the heart
  • Contractility
    • Inotropy
    • Force produced during contraction at a given preload
    • Influences End Systolic Volume (↑Contractility = ↓ESV)


  • Back pressure exerted by arterial blood
  • The tension needed by ventricular contraction to open semilunar valve
    • i.e., The pressure the heart must reach to eject blood
  • ↑Afterload = ↑ESV = ↓SV
  • Afterload is increased by anything that restricts arterial blood flow


Relationship between Flow, Pressure, Resistance

  • Flow is directly proportional to pressure gradient between 2 points (change in pressure)
  • Flow is inversely proportional to resistance
  • Resistance is far more important in determining local blood flow versus the pressure gradient 

Blood Flow Rate 

  • The Amount of blood flowing through a vessel/organ/system per unit time (mLs/min)
    • Determined by pressure gradient & resistance, NOT velocity
  • Systemic Blood Flow = Cardiac Output (relatively constant)
  • Specific Organ Blood Flow – may vary widely due to its immediate needs

Velocity of Flow 

  • Velocity of Flow = SPEED of flowing blood (mm/sec)
  • e..g, A constricted vessel will have a lower flow rate, but a higher velocity of flow (i.e., Garden hose)
  • Note: Velocity tends to change by a greater magnitude than the change in Flow Rate

Blood Pressure

  • The Pressure exerted on the vessel wall by contained blood (mmHg)
  • Decreases with distance from heart (arterial system)
  • Decreases with 10%+ decrease blood volume
  • Increases with vessel constriction (provided same blood volume)


  • The amount of friction blood encounters as it passes through the vessels
  • 3 factors influencing resistance
    • Blood Viscosity (↑Viscosity = ↑Resistance) (Fairly Constant)
    • Total Vessel Length (longer vessel = ↑ resistance) (Fairly Constant)
    • Vessel Diameter (thinner vessel = ↑resistance) (Frequently Changes)
      • Most responsible for changes in BP
  • Systemic Vascular Resistance = Combination of the Above Factors

Effects of Vessel Diameter (Vasomotion) on Flow Rate 

  • The flow rate is directly proportional to the 4th power of the vessel diameter
  • i.e., Small changes in vessel diameter → Changes flow rate by an exponent of 4
  • Poieuille’s Law 

Effects of Vessel Diameter (Vasomotion) on Flow Velocity

  • Flow rate is inversely proportional to the vessel’s cross-sectional area
  • i.e., An ɑ x increase in cross-sectional area → decrease in flow velocity by a factor of ɑ

Blood Pressure Physiology

Factors Influencing Blood Pressure

  • Cardiac Output
    • ↑Cardiac Output = ↑ BP
  • Peripheral Resistance
    • Causes back pressure in blood (arterial system)
    • e.g., In obesity, peripheral resistance increases.
  • Blood Volume
    • (assuming constant vessel diameters) ↑Blood Volume = ↑BP
    • Its effect depends on vessel compliance

BP = Cardiac Output X Total Peripheral Resistance

Types of Blood Pressure


  • Peak aortic pressure reached during ventricular systole
  • A function of
    • Peak rate of ejection
    • Vessel wall compliance
    • Diastolic BP
  • Normal = 120mmHg


  • Lowest aortic pressure reached during ventricular diastole, due to blood left after peripheral runoff
  • A function of
    • Blood volume
    • Heart rate
    • Peripheral resistance
  • Normal = 80mmHg

Pulse Pressure*

  • Pulse Pressure = Systolic Pressure – Diastolic Pressure
  • e.g., 120mmHg – 80mmHg
  • Normal = 40mmHg
  • If lower: may be an indication of Aortic Stenosis or Atherosclerosis (slowed peripheral runoff)

Mean Arterial Pressure*

  • MAP = Diastolic Pressure + 1/3(Pulse Pressure)
  • The pressure that propels blood to the tissues – maintains tissue perfusion
    • Maintains flow through capillary beds
  • Must be high enough to overcome peripheral resistance (if not, blood doesn’t move)
  • Finely controlled

3 Main Regulators of Mean Arterial Pressure

Autoregulation (at the tissue level) 

  • Localized automatic vasodilation/constriction at the tissue level
    • Allows control of flow within a single capillary bed
    • Ensures perfusion of the ‘needy’ tissues
  • Metabolic controls → Vasodilation
    • Low oxygen/nutrient levels
    • Nitric Oxide
    • Endothelin
    • Inflammatory chemicals: histamine/kinins/prostaglandins
  • Myogenic control → Vasoconstriction
    • Sheer stress: Vascular smooth muscle responds to passive stretch (↑vascular pressure) with increased tone
      • Prevents excessively high tissue perfusion that could rupture smaller blood vessels
    • Reduced stretch promotes vasodilation → flow increases

Neural Mechanisms

  • Vasomotor Center (medulla) 
    • Take info from receptors
      • Baroreceptors (primarily)
      • Chemoreceptors (lesser degree)
    • Transmit impulses via sympathetic nervous system
      • ↑ sympathetic activity = vasoconstriction = ↑ BP
      • ↓ sympathetic activity = vasodilation = ↓ BP
  • Cardiovascular Centers of the ANS 
    • Sympathetic → ↑HR & Contractility → ↑MAP
    • Parasympathetic → ↓Heart Rate → ↓MAP

Endocrine Mechanisms (Kidney Level) 

  • More for long-term BP & blood-volume regulation
  • Antidiuretic Hormone (ADH)
    • Aka vasopressin
    • Released due to low blood volume
    • ADH → Water Retention Increased → ↑MAP
  • Angiotensin II
    • Released due to low blood pressure
    • Potent vasoconstrictor
    • Increases cardiac output & blood volume
    • Angiotensin II → Vasoconstriction → ↑MAP
  • NOTE: ‘ACE’ (Angiotensin I Converting Enzyme) activates it to Angiotensin II. Hence ‘ACE-Inhibitors’ are often used as AntiHypertension medicine)
  • Erythropoietin
    • Released due to low pressure & low O2 levels
    • Increases RBC production to increase blood volume
    • EPO → Hematopoiesis → ↑Blood Volume → ↑MAP
  • Natriuretic Peptides (Released by the heart)
    • Released by the heart due to high blood pressure & volume
    • ↑Stretch on Heart → NP Release → ↑Diuresis → Reduces BP & Volume
    • Also inhibits ADH & Angiotensin II → Reduces BP & Volume

Anatomy & Physiology of Blood Vessels

Introduction to Blood Vessels

3 Classes

  • Arteries → carry blood away from the heart
    • Elastic Arteries
      • e.g., Aorta & major branches (Conducting Vessels)
    • Muscular Arteries
      • e.g., Coeliac trunk & renal arteries (Distributing Vessels)
    • Arterioles
      • e.g., Intra-organ arteries (Resistance Vessels)
    • Terminal Arteriole
      • e.g., Afferent arteriole in kidney
  • Capillaries → intimate contact with tissue; facilitate cell nutrient/waste transfer
    • Vascular shunt
    • True capillaries
  • Veins → carry blood back to the heart
    • Post-capillary venule (union of capillaries) 
    • Small veins & large veins
      • Capacitance vessels
      • 65% of body’s blood is venous

Relationships between Vessel Diameter, Cross-Sectional Area, Local Blood Pressure, and Velocity of Flow 

Blood Vessel Structure

3-layered wall 

Tunica Intima 

  • i.e.,  The layer in intimate contact with the blood (luminal)
  • Consists of the endothelium (simple squamous epithelium)
  • Larger vessels also have a sub-endothelial layer

Tunica Media

  • Middle and thickest layer (smooth muscle + elastin)
    • Circulating smooth muscle
    • Sheets of elastin
  • Regulated by sympathetic nervous system + chemicals
  • Contraction/dilation maintains blood pressure

Tunica Externa

  • Outermost layer (Loose collagen fibers)
  • NOTE: Also contains nerve fibers, lymphatics, and vasa vasorum (in larger vessels)

The Arterial System

Elastic (Conducting) Arteries

  • The aorta + its major branches
  • Thick-walled
  • Large lumen = low resistance
  • Highest proportion of elastin
    • Withstands pressure fluxes
    • Smooths out pressure fluxes
    • ‘Stretch’ = potential energy → helps propel blood during diastole

Muscular (Distributing) Arteries 

  • Distal to elastic arteries
  • Deliver blood to specific body organs
  • Diameter: 0.3mm→1cm
  • Thickest tunica media
    • Due to smooth muscle
  • Highest proportion of smooth muscle
    • Are active in vasoconstriction
    • Are therefore less distensible (less elastin)


  • Smallest arteries
  • Larger arterioles have all 3 tunics (intima/media/externa)
    • Most of the tunica media is smooth muscle
  • Smaller Arterioles
    • Lead to capillary beds
    • Little more than 1 layer of smooth muscle around the endothelial lining
  • Autoregulation of diameter
    • Controlled by
      • Neural (electrical) signals
      • Hormonal signals
        • Noradrenaline
        • Epinephrine
        • Vasopressin
        • Endothelin-1
      • Local chemicals
    • Controls blood flow to capillary beds
      • When constricted – tissues served are bypassed
      • When dilated – tissues served receive blood
  • Biggest controller of blood pressure

The Capillary System

  • Smallest blood vessels – microscopic
  • Thin, thin walls 
  • Tunica intima only (i.e., only 1 layer thick)
  • Average length = 1mm
  • Diameter: the width of a single RBC
    • RBC’s flow through capillaries in single file
    • RBC’s shape allows them to stack up efficiently against each other
  • Penetrate most tissues, except:
    • Tendons
    • Ligaments
    • Cartilage
    • Epithelia
  • Main role
    • Exchange of gases/nutrients/hormones/wastes
    • Exchange occurs between blood & interstitial fluid

Capillary Beds

  • Capillaries are only effective in large numbers
    • Form networks called ‘capillary beds’
  • Facilitates microcirculation
    • Blood flow from an Arteriole → Venule
    • Consist of 2 types of vessels
      • Vascular Shunt
        • From metarteriole → thoroughfare channel
        • Short vessel – directly connects arteriole with venule
      • True Capillaries
        • The ones that actually take part in exchange with tissues
        • Usually branch off the metarteriole (proximal end of vascular shunt)
        • Return to the thoroughfare channel (distal end of vascular shunt)
        • Precapillary Sphincters
          • Smooth muscle cuffs
          • Surround the roots of each true capillary (arterial ends)
          • Regulates blood flow into each capillary
          • i.e., Blood can either go through capillary or through the shunt
  • A capillary bed may be flooded with blood or bypassed, depending on conditions in that organ

3 Types of Capillaries

Continuous Capillaries

  • ‘Continuous’ = uninterrupted endothelial lining
  • Adjacent cells form intercellular clefts
    • Joined by incomplete-tight-junctions
    • i.e., Allow limited passage of fluids & solutes
  • NOTE: In the brain, the tight-junctions are complete → blood brain barrier

Fenestrated Capillaries 

  • Endothelial cells are riddled with oval pores (fenestrations = windows)
    • Much more permeable to fluids & solutes than continuous capillaries
  • Abundant wherever active absorption/filtration occurs
    • Intestines
    • Kidneys
    • Endocrine organs (allow hormones rapid entry to blood)

Sinusoids (Sinusoidal Capillaries) 

  • aka  “leaky capillaries”
  • Found ONLY in
    • Liver
    • Bone marrow
    • Lymphoid tissues
    • Some endocrine organs
  • Large irregularly-shaped lumens
  • Usually fenestrated
  • ‘Discontinuous’ = interrupted by Kupffer cells
    • Remove & destroy bacteria
  • Intercellular clefts → larger + have fewer tight junctions
    • Allow large molecules & leukocytes passage through to interstitial space

The Venous System

  • Vessels carry blood back towards the heart (from capillary beds)
  • Vessels gradually increase in diameter & thickness towards the heart

2 Types


  • Formed by union of capillaries (post-capillary venules)
  • Consist entirely of endothelium
  • Extremely porous
  • Allows passage of
    • Fluid 
    • White blood cells (migrate through wall into inflamed tissue)
  • The larger venules
    • Have 1 or 2 layers of smooth muscle (i.e., tunica media)
    • Have a thin tunica externa as well


  • Formed by union of venules
  • 3 distinct tunics (but walls thinner than corresponding arteries)
    • Thinner walls due to lower blood pressure
  • Tunica media
    • Poorly developed
    • Some smooth muscle
    • Some elastin
    • Tend to be thin even in large veins
  • Tunica externa
    • Heaviest layer (thicker than media)
    • Thick longitudinal collagen bundles
    • Thick elastic networks
  • Lumens larger than corresponding arteries
    • The reason 65% of the body’s blood is in the veins
    • Therefore veins: aka “capacitance vessels”
  • Lower blood pressure than arteries
    • Require structural adaptations to get blood → heart:
      • Large lumen (low resistance)
      • Valves
  • Venous valves
    • Folds of tunica intima (resemble semilunar valves)
    • Prevent blood flowing backward
    • Ensures unidirectional flow
    • Often have to work against gravity
    • If faulty, causes thrombosis (e.g., varicose veins)

Fetal Circulation 

  • “Bypasses” / “shunts” of fetal circulatory system
  • All of these “shunts” are occluded at birth due to pressure changes

Ductus Venosus

  • Directs the oxygenated blood from the placental vein into inferior vena cava → heart
  • Partially bypasses the liver sinusoids

Foramen Ovale

  • An opening in the interatrial septum loosely closed by a flap of tissue
  • Directs some blood entering the right atrium into the left atrium → aorta
  • Partially bypasses the lungs
  • NOTE: Foramen ovale can take up to 6 months to close 

Ductus Arteriosus

  • Directs most blood from right atrium of the heart directly into aorta
  • Partially bypasses the lungs

Fluid Movements across a Vessel

  • Determined by the balance of 2 forces
  • Hence, fluid is forced out at arterial end, and reabsorbed at venous end
  • The amount of fluid forced out = determined by the balance of net hydrostatic & osmotic forces
    • i.e., Net Filtration Pressure = Net Hydrostatic Pressure – Net Osmotic Pressure 

Capillary Hydrostatic Pressure

  • The force the blood exerts against the capillary wall
  • Hydrostatic pressure = capillary blood pressure ≈ 35 mmHgArterial End /15 mmHgVenous End
  • Tends to force fluids through the capillary’s intercellular clefts (between endothelial cells)
    • Capillary hydrostatic pressure drops as blood flows from arteriole → venule
  • Net hydrostatic pressure = Capillary Hydrostatic Pressure – Interstitial Hydrostatic Pressure
    • NOTE: Interstitial Hydrostatic Pressure ≈ 0 mmHg

Colloid Osmotic Pressure

  • Opposes hydrostatic pressure
  • Due to large, non-diffusible molecules (plasma proteins) drawing fluid into capillaries
  • Typically ≈ 25 mmHg
    • Relatively constant at both arterial & venous ends
  • Net Osmotic Pressure = Capillary Osmotic Pressure – Interstitial Osmotic Pressure
    • NOTE: Interstitial Osmotic Pressure ≈ 1 mmHg


  • Abnormal accumulation of fluid in the interstitial space (i.e., tissue swelling)
  • Caused by increase in flow of fluid → out of vessel or lack of reabsorption → into blood vessel
  • Usually reflects an imbalance in colloid osmotic pressure on the 2 sides of the capillary membrane
    • e.g., Low levels of plasma protein (reduces amount of water drawn into capillaries
  • Contributing factors
    • High BP (Hydrostatic Pressure)
      • Can be due to incompetent valves
      • Localized blood vessel blockage
      • Congestive heart failure (pulmonary edema – due to blockage in pulmonary circuit)
      • High blood volume
    • Capillary Permeability
      • Usually due to an inflammatory response

Injuries to Blood Vessels


  • Formation of fatty plaques in the subendothelial layer
  • Fatty plaques begin to ulcerate 


  • Elastic arteries can lose their elasticity 
  • Due to having thinner walls, they’re more prone to aneurysm formation (bulging & potentially rupturing)
    • Result in pooling of blood → eventual rupture 


  • Blood builds up between the layers of the wall & eventually press the vessel closed

 Physiology of Hypertension

What is Hypertension? 

  • Consistent diastolic of +90mmHg AND/OR 
  • Consistent systolic of +140mmHg
  • A risk factor for other diseases
    • Coronary artery disease 
    • Stroke 
    • Heart failure 
    • Renal failure
    • Peripheral vascular disease 
  • Usually asymptomatic 
  • Often misdiagnosed due to 
Factor Effect on BP Reading
Cuff – too wide/long Lower than actual 
Cuff – too narrow/short Greater than normal 
Arm – above heart Lower than normal 
Arm – below heart Greater than normal 
Arm – unsupported Greater than normal
Respiration rate Lower during inspiration
“White coat” phenomenon  Much greater than normal 
Smoking/caffeine/activity 30 minutes prior to reading Greater than normal 

Classifications Based on BP Ranges 

Category Systolic Diastolic % Population
Normal <130 <85 83
Pre-hypertensive 130-139 85-89
Stage 1 Hypertension 140-159 90-99 13.5
Stage 2 Hypertension 160-179 100-109 2
Stage 3 Hypertension 180-209 110-119
Stage 4 Hypertension  >210  >120 1

2 Types of Hypertension (based on etiology) 

Primary (Essential) Hypertension 

  • 90-95% of cases
  • No specific cause
  • Related to
    • Obesity
    • ↑Cholesterol
    • Atherosclerosis
    • ↑Salt Diet
    • Diabetes
    • Stress
    • Family History
    • Smoking
  • Diastolic Hypertension
    • Elevated diastolic pressure
    • Relatively normal systolic (or slightly elevated)
    • Mostly middle-aged men
  • Isolated Systolic Hypertension
    • Elevated systolic pressure
    • Normal diastolic pressure
      • i.e., High Pulse Pressure
    • In older adults (60 years+)
      • May be due to reduced compliance of the aorta with increasing age
    • In younger adults (17-25 years)
      • May be due to overactive sympathetic NS → ↑Cardiac Output
      • Or congenitally stiff/narrow aorta

Secondary (Inessential) Hypertension

  • 5-10% of cases 
  • Secondary to another disease, e.g.:
    • Renal disease 
    • Endocrine disorders 
    • Pregnancy (pre-eclampsia)
      • In 10% of pregnancies 
      • 20 weeks of gestation 
    • Others: cancer, drugs, alcohol 

Organ Damage Caused by Hypertension 


  • Increased afterload
    • ↑ Workload of Heart → ↑Afterload → Pumps Harder → Hypertrophy → Failure
  • Left ventricular hypertrophy
    • To compensate for higher workload
    • Compromised L-Ventricular Volume → ↓Stroke Volume →↓Cardiac Output


  • Pulmonary congestion 
  • Backing up of blood in pulmonary circuit 
  • Why? ↑BP = ↑Aortic-BP = ↑Afterload = ↓SV = ↑ESV = ↓Pulmonary Blood Flow


  • Stroke – typically intracerebral hemorrhage 
  • Rupture of artery/arterioles in the brain 

See image on right-hand side

Aorta/Peripheral Vascular 

  • Arterial mechanical damage (e.g., aneurysms/dissecting aneurysms) 
  • Accelerated atherosclerosis


  • Nephrosclerosis (hardening of kidney blood vessels) 
  • Renal failure 

Short-term Physiological Control of Blood Pressure 

The Baroreceptor Reflex 

Risk Factors of Hypertension 


  • Blood pressure normally increases with age
    • Baby: 50/40
    • Child: 100/60
    • Adult: 120/80
    • Aged: 150/85 (quite normal) 
  • Due to the loss of elasticity of blood vessels (decreased compliance) 
  • Atherosclerosis 



  • Fatty diet → atherosclerosis
  • Body fat → kms more vessels → ↑Peripheral Resistance → Hypertension
  • Physical weight of fat may impede venous return
  • Kidney dysfunction → loss of long-term BP (blood volume) control

Excess Na+ Intake 

  • If normal kidney function
    • Na+ intake → slight BP increase (due to fluid retention) 
    • But excess Na+ intake and H2O excreted by kidneys → BP returns to normal 
  • If impaired kidney function
    • Na+ intake → larger BP increase 
    • Because excess Na+ and H2O not excreted by kidneys (less efficiently) 

Basic Hypertension Treatment Plan

Anti-Hypertensive Drug Mechanisms 

  • Diuretics
    • Increase urination → decrease blood volume 
    • Aim: reduce workload on heart by reducing preload 
  • Sympatholytics
    • Reduces sympathetic activity (Prevents ↑HR/↑Contractility = Decrease in CO)
    • e.g., beta blockers 
  • Vasodilators
    • Reduce peripheral resistance
    • Reduce afterload
    • Reduce workload on the heart 
  • Renin-Angiotensin Antagonists (ACE Inhibitors)
    • Decreases effects of Renin-Angiotensin System
      • Decreases sympathetic drive 
      • Decreases vasoconstriction
      • Decreases fluid retention
      • Decreases preload 
      • Decreases afterload 

Physiology of Shock


  • Profound hemodynamic/metabolic disorder due to inadequate blood flow and O2 delivery 
  • Common causes of shock 
    • Hypovolemic change
      • Severe dehydration 
      • Hemorrhage 
    • Cardiogenic change
      • Heart failure (heart isn’t getting enough blood out) 
      • Decreased venous return 
    • Distributive alteration
      • Excessive metabolism (i.e., even a normal CO is inadequate) 
      • Abnormal perfusion patterns (i.e., most of CO perfuses tissues other than those in need) 
      • Neurogenic shock (i.e., sudden loss of vasomotor tone → massive venodilation) 
      • Anaphylactic shock (drastic decrease in CO & BP due to allergic reaction) 
      • Septic shock (disseminated bacterial infection in the body → extensive tissue damage) 

3 Stages of Shock 


  • Stable, not self-perpetuating
  • Symptoms
    • Hypotension (Low BP)
    • Tachycardia (High HR – body’s attempt to compensate for poor perfusion)
    • Tachypnea (High breathing-rate – phrenic nerve stimulation – diaphragm)
    • Oliguria (Low urine production by kidney)
    • Clammy skin
    • Chills
    • Restlessness
    • Altered consciousness
    • Allergy symptoms (if anaphylaxis)
  • The body’s compensatory mechanisms (below) will prevail without intervention.
    • Aim to increase BP

Progressive Stage 

  • Unstable, vicious cycle of cardiovascular deterioration – self-perpetuating
  • Compensatory mechanisms are insufficient to raise BP
  • Perfusion continues to fall → organs become more ischemic (heart → failure)
    • Cardiac depression (due to O2 Deficit to Heart)
    • Vasomotor failure (due to O2 Deficit to Brain)
    • “Sludged blood” (viscosity ↑ – harder to move)
    • Increased capillary permeability
  • Symptoms
    • Beginning of organ failure
    • Severely altered consciousness
    • Marked bradycardia (initially tachycardic – but now the body is giving up)
    • Tachypnea (fast breathing) with dyspnea (no breathing)
    • Cold, lifeless skin
    • Acidosis – (CO2 equation affected)
  • Treatment
    • Identify & remove causative agents
    • Volume replacement for hypovolemia
    • If septic shock: antibiotics
    • Sympathomimetic drugs: if neurogenic shock (loss of vasomotor tone – vasodilation)
  • Fatal if untreated

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